Gene interactions and pathways from curated databases and text-mining

◀ Back to IL1A

ACAN — IL1A

Text-mined interactions from Literome

Patwari et al., Arch Biochem Biophys 2000 : In this study we examined the effect of ManN and GlcN on aggrecanase mediated degradation of aggrecan induced by IL-1alpha and the corresponding tissue mechanical properties in newborn bovine articular cartilage
Nishida et al., Arthritis Rheum 2000 : To determine the effects of interleukin-1alpha (IL-1alpha) on the expression of hyaluronan synthase (HAS), CD44, and aggrecan in human articular chondrocytes, and to assess the net result of these metabolic changes on the accumulation of hyaluronan within articular cartilage
Pfander et al., Ann Rheum Dis 2004 (Osteoarthritis, Knee) : To analyse the distribution patterns of tenascin and proteoglycans in normal and osteoarthritic cartilage, and to determine the effect of interleukin 1beta (IL1beta) on aggrecan and tenascin expression by human articular chondrocytes in vitro
Arai et al., Osteoarthritis Cartilage 2004 : Analysis of bADAMTS-4 transcriptional regulation in chondrocytes revealed that interleukin-1alpha (IL-1alpha) was the most potent inducer of bADAMTS-4 mRNA and subsequent aggrecan degradation in cartilage explant cultures of those cytokines tested
Radons et al., Int J Mol Med 2006 : p38MAPK mediates IL-1 induced down-regulation of aggrecan gene expression in human chondrocytes ... IL-1 induced down-regulation of aggrecan expression was found to be mediated by p38MAPK and/or ERK1/2
Pratta et al., Osteoarthritis Cartilage 2006 : We also observed that the basal, as well as IL-1 stimulated production of ARGS aggrecan fragments from human articular cartilage explants was blocked by a selective aggrecanase inhibitor, consistent with generation of the ARGS neoepitope in human articular cartilage being mediated by aggrecanase
Ilic et al., J Biol Chem 2007 : IL-1alpha and retinoic acid stimulated radiolabeled aggrecan loss from wild-type and ADAMTS-4 Deltacat cartilage, but there was little effect on ADAMTS-5 cartilage ... Retinoic acid, but not IL-1alpha , stimulated radiolabeled aggrecan loss from ADAMTS-4/-5 Deltacat cartilage explants
Rogerson et al., Arthritis Rheum 2008 : TS-4/TS-5 Delta-cat cartilage explants did not release aggrecan in response to IL-1alpha , and there was no detectable increase in aggrecanase neoepitopes
Wang et al., Growth Factors 2009 : FGF2, IL-1beta , and TSA inhibited expression of aggrecan , while TSA also decreased mRNA levels of collagen type II
Akhtar et al., BMC complementary and alternative medicine 2011 (Osteoarthritis) : Effect of HLM on IL-1ß induced gene expression of iNOS, MMP-9, MMP-13, ACAN and COL2A1 was verified by real time-PCR ... The objective of this study was to investigate the anti-inflammatory/chondroprotective potential of a Herbal and amino acid mixture containing extract of the Uncaria tomentosa, Boswellia spp., Lepidium meyenii and L-Leucine on the IL-1ß induced production of nitric oxide ( NO ), glycosaminoglycan ( GAG ), matrix metalloproteinases ( MMPs ), aggrecan (ACAN) and type II collagen ( COL2A1 ) in human OA chondrocytes and OA cartilage explants
Gilbert et al., European cells & materials 2012 : OSM+IL-1 reduced the expression of COL2A1 ( type II collagen ), COL9A1 ( type IX collagen ), COL11A1 ( type XI collagen ), and ACAN ( aggrecan ) mRNAs
Wei et al., Spine (Phila Pa 1976) 2013 : ERK inhibition reversed the changes of protein expression of MMP-3, MMP-13, TIMP-1, aggrecan and collagen II induced by IL-1
Thumb et al., Wien Med Wochenschr 1995 (Osteoarthritis) : IL-1 stimulates the production of proteolytic enzymes and inhibits the synthesis of aggrecan and leads therefore to a degradation of the cartilage
Fukuda et al., Inflamm Res 1995 : We investigated the importance of prostaglandin E2 ( PGE2 ) release in interleukin-1 (IL-1) induced inhibition of aggrecan synthesis by chondrocytes
Chandrasekhar et al., Agents Actions Suppl 1993 : The results suggest that while IL-1 affects both increased aggrecan loss and decreased synthesis, the pathways leading to the effector functions are not necessarily linked and are likely to be distinct